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Progesterone Reduces Pentylenetetrazol‐Induced Ictal Activity of Wild‐Type Mice But Not Those Deficient in Type I 5α‐Reductase
Author(s) -
Frye Cheryl A.,
Rhodes Madeline E.,
Walf Alicia,
Harney Jacob
Publication year - 2002
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.43.s.5.19.x
Subject(s) - pentylenetetrazol , endocrinology , medicine , reductase , enzyme , knockout mouse , wild type , chemistry , pharmacology , epilepsy , biology , anticonvulsant , receptor , biochemistry , mutant , psychiatry , gene
Summary: Purpose: To investigate the importance of progesterone (P 4 ) metabolism by the 5α‐reductase type I enzyme in mitigating P 4 antiseizure effects. Methods: Ovariectomized, female homozygous and heterozygous 5α‐reductase type I knockout mice (n = 23) and their wild‐type siblings (n = 31) were administered P 4 (1.0 mg), and their pentylenetetrazol (PTZ)‐induced ictal behaviors were compared with those of vehicle‐administered mice (n = 49). Results: Mice deficient in the 5α‐reductase type I enzyme administered P 4 , or vehicle‐administered control mice, had significantly shorter latencies and increased incidence of PTZ‐induced hindlimb extension and death than did wild‐type mice administered P 4 . Conclusions: These data suggest that P 4 's metabolism by the 5α‐reductase type I enzyme may mitigate some of P 4 's antiseizure effects in the PTZ‐induced seizure model.